The lumbar intervertebral disc is the largest avascular structure in the human body. A bipedal posture forces the spine into an S-shape curve. The goal is to maintain the skull centered over the pelvis. This has resulted in a lordotic lumbar spine. Degenerative changes in the lumbar discs are typically ubiquitous it is considered a normal part of aging. These degenerative changes have been documented on several MRI scan studies. Gravity creates a compressive load upon the intervertebral discs, and spinal motion creates shear forces and damage from vibration. Mechanical loading cannot in itself explain the ubiquitous degenerative changes seen in the human discs. Various animal studies have been contradictory when it comes to a direct correlation between mechanical stress and disc degeneration. Likewise, human studies attempting to link disc degeneration directly to mechanical factors such as heavy physical work have failed to make a direct correlation.
The cartilage cells living in the avascular lumbar disc receive nutrition through an extracellular matrix with an attenuated supply of nutrients through the vertebral endplates. Nutrients must travel through the capillary network in the intervertebral body and then diffuses through the endplate into the extracellular matrix and finally to the cartilage cells. Calcification of the endplates impairs the flow of nutrients such as glucose and oxygen. Endplate calcification exacerbates the hypoxic acidic environment that greatly impairs the cartilage cell metabolism. The hypoxic acidic environment results in a decrease in proteoglycan synthesis and a cascade of cartilage cell death. The decrease in proteoglycan production is the prevalent feature of disc degeneration. The primary degrading enzyme is the matrix metalloproteinases (MMPs). The MMPs degrade not only the collagens present in the matrix and Aggrecans. Cathepsins are other proteinases associated with disc degeneration that degrade collagen and proteoglycans along with the MMPs. Cathepsins are found more in an acidic pH and may be the primary proteinase in disc degeneration. Degenerated cartilage cells also produce various pro-inflammatory mediators such as leukotriene B4, thromboxane B2, prostaglandin E2, phospholipase A2 and COX-2.
Thus, there remains a need for a point-of-care, autologous cell based therapy that can be implemented with minimal manipulation of the extracted cells and retention of the physiologic regenerative attributes present within the microenvironment of the cellular extract. The present novel technology addresses this need.